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pharm Flashcards

1
Q

histamine triple response

A

red - vasodilation
wheal - increase permeabilty
flare - spreading response through sensory neurons

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2
Q

how does histamine cause acid secretion

A

acts on H2 R on parietal cell, to increase cAMP

activates K/H pum p

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3
Q

biosynthesis of bradykinin

A

prekallikrein converted to kallikrein by factor XII

kallikrein converts HMW kinninogen to bradykinin

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4
Q

C1 esterases

A

kallikreins

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5
Q

hereditary angioedema

A

deficiency in CI esterase inhibitor - use B2 R ant

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6
Q

activation and effects of NO

A

ach/bradykinin/sheer stress - causes increase Ca
Ca activates nitric oxide synthase
converts arginine to NO
NO activates guanylate cyclase to increase cGMP and cause relaxation

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7
Q

what regulates vascular tone

A

basal release of NO

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8
Q

symp or parasymp has greater influence on HR at rest

A

parasymp

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9
Q

symp action on heart

A

act on B1, increase cAMP, opens Ca channels - decrease time to reach potential, increase rate of firing, increase conduction time

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10
Q

3 mechanisms underlying dysrhythmias

A
  1. altered pulse formation - abnormal AP generation
  2. altered pulse conduction - conduction block, re-entry
  3. triggered activity - early or late afterdepolarisations:
    - early - abberant Na or Ca channel opening
    - late - Ca overload - excitation on completion of repolarisation
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11
Q

4 Classes of antidysrhythmics

A
  1. Na channel blockers - 1a, b,c
  2. B blockers
  3. K channel blockers
  4. Ca channel blockers
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12
Q

class 1 a b c antidysrhythmics

A

Na channel blockers
1a - quinidine - moderate block, prolong repolarisation, increase ERP
1b - lignocaine - mild block, shorten repolarisation, decrease ERP
1c - flecainide - big block, same repolarisation, same ERP

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13
Q

amiodarone

A

K channel blocker, also other ones

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14
Q

antihypertensives

A

a - angiotensin system inhibitors - Ace inhibitors, AngiR ants
b - B antagonists
c - L-type Ca blockers
d - diuretics

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15
Q

olols

A

B blockers

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16
Q

sartans

A

angI R ant

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17
Q

prils

A

ACE inhibitors

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18
Q

digoxin mehcanism of action

A

inhibits Na/K atpase, increase Na intracellular, decreases Ca extrusion - builds up in SR, increase Ca release with each AP

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19
Q

dobutamine

A

B agonist

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20
Q

heparin

A

enhances antithrombin 3 activity - inactivates factor Xa and thrombin

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21
Q

monitoring of heparin with

A

APTT

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22
Q

warfarin

A

inhibits vit K reductase - inhibits reduction of vit K, therefore inhibits gamma carboxylation in blood coagulation factors

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23
Q

monitor warfarin with

A

PT and INR

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24
Q

3 drugs affecting platelet activation/adhesion

A

ADP R ant
aspirin
GPIIb/IIIa R ant

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25
Q

fibrinolytic drugs

A

streptokinase

alteplase - hrtPA - clot selective, not antigenic

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26
Q

loop diuretics mech of action

A

block Na/K/Cl carrier in thick ascending limb

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27
Q

thiazide diuretics mech

A

inhibit Na/Cl in distal tubule

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28
Q

side effects of thiazide

A

K loss, increase uric acid

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29
Q

loop diuretics side effect

A

K loss, H loss - metabolic alkalosis

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30
Q

K Sparing diuretics mech

A

spironolactone - ald R ant - block Na channels and decreased Na/K pump synthesis
amiloride - Na luminal channel blocker

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31
Q

3 drugs that can damage kidney

A

mercury - toxicity and vasoconstriction
gentamicin - alters Ca metabolism
cisplatin - forms ROs

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32
Q

statins mech

A

HMG-CoA reductase inhibitors - decrease cholesterole synth so increase LDL R on liver and increase LDL uptake and increase HDL

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33
Q

bile acid sequestrants

A

prevent absorption cholesterol, increase excretion, increase demand for chol for bile acid syntheiss, increase LDL R adn removal of LDL

34
Q

Ezetimibe

A

inhibits sterol transporter in intestine - only as adjacent to statin

35
Q

treatment for hypertriglyceridaemia

A

fibrates - increase LPL so decrease TAGs in plasma

36
Q

nicotinic acid

A

hypercholesterolaemia treatment - all statin things plus decreases atherogenic lipoprotein a - but poor tolerance

37
Q

4 treatments for stable angina

A
  1. nitrates - No release
  2. Ca channel blockers - decrease afterload, HR, SV
  3. B blockers
  4. ivabradine
38
Q

unstable angina treatment

A

as for stable plus aspirin

39
Q

process of mast cell degranulation

A

FcR clustering - tyrosine K activity - PLC - Dag (PKC) and IP3 (Ca mobilisation) - degranulation

40
Q

where cys-LT released from

A

eosins, masts, macs

41
Q

cys-LT physiological role or path

A

only path

42
Q

endogenous mast cell inhibitors

A

PGE2, Adrenaline, cortisol

43
Q

disodium chromoglycate

A

causes annexin-1 releaes - inhibits cys-LT production

44
Q

omalizumab

A

binds IgE

45
Q

montelukast

A

cys-LT R ant for aspirin or exercise induced asthma

46
Q

asthma airway hyperresponsiveness

A

airways constrict too easily and too much

47
Q

SABA mech of action

A

B2 ag - Gs - PKA - activates SERCA, blocks Ip3 - both decrease Ca intracellular - decrease contraction

48
Q

treatment of bronchoconstriction in COPD

A

anti-musc

49
Q

actions of glucocorticoids in asthma

A
  • decrease activity, recruitment, survival of eosins and Th2
  • decrease mast cell activation and cytokine production
  • decrease prolif, cyt and collagen production of smooth muscle adn fibroblasts
50
Q

indication for inhaled GCS

A

if B2 ag needed more than 3 times a week

51
Q

cell infiltration in COPD

A

neuts, CD8, lots of macs

52
Q

Triple wammy

A

ace inhibitor - dilate efferent arteriole
diuretic - decrease volume
NSAID - vasoconstrict afferent arteriole

53
Q

methotrexate

A

blocks human dihydrofolate reductase - anticancer, immunosuppressant

54
Q

amphotericin

A

stops ergosterol synthesis - antifungal

55
Q

paclitaxel

A

bind polymerised tubulin - prevents dissassembly therefore mitosis - anti cancer

56
Q

short term infusion useful for what drugs

A

low TI

57
Q

problem with low bioavailability

A

patient variability will have higher consequences

58
Q

problem with slowly distributing drug

A

peak conc will be higher than expected based on Vd as in beginning its distributing in smaller compartment as hasnt reached fat or muscle yet

59
Q

newborns deficinet in what metabolism enzymes

A

phase II

60
Q

elderly deficient in what metabolism enzymes

A

phase I - CYT

61
Q

what is pharmacokinetic drug drug interaction

A

drug a effects conc of drug b at receptor

62
Q

what is pharmacodynamic drug drug interaction

A

drug a effects actions of drug b without altering conc at R

63
Q

esomeprazole

A

PPI - H/K atpase - PUD

64
Q

ranitadine

A

H2R ant - PUD

65
Q

sodium bicarb

A

antacids

66
Q

hyoscine butylbromide

A

musc R ant - smasmolytic

67
Q

misoprostol

A

PGE2 anaolgue

68
Q

promethazine

A

H1R ant - antiemetic - motion sick

69
Q

hyoscine hydrobromide

A

M R ant - anti-emetic

70
Q

metoclopramide

A

D2R ant (also blocks 5HT3 and 4 )- anti-emetic

71
Q

prochlorperazine

A

D2R ant - less sedative - anti-emetic, extrapyramidal side effects

72
Q

ondansetron

A

5HT3 R ant - antiemetic - no extrapyramidal side effects

73
Q

aprepitant

A

NK1R ant - anti-emetic

74
Q

4 laxatives

A

bulking agents
faecal softeners and lubricants - docusate
magnesium sulphate - osmotic laxative
senna - stimulant

75
Q

antidiarrhoeals

A

loperamide - opioid
mebeverine - anti-spasmolytic
hyoscine butylbromide - anti-spasmolytic

76
Q

treatment for gas

A

simethicone - defoaming agent
activated charcol
carminatives - peppermint, dil

77
Q

two types of dose dependent side effects

A

on target and off target

78
Q

what problem with terfenadine and grapefruit

A

terfenadine usually 0% bioavailable and converted to active metabolite
grapefruit competitively binds to CYP3A4 - terf becomes bioavailable and inhibits K channels - fatal ventricular arrhythmias

79
Q

2 metabolism pathways of paracetamol

A
  1. conjugated to suphate or glucoronide metabolite

2. oxidised by CYP450 into intermediate metabolite and glutathione conjugates into non-toxic product

80
Q

why does paracetamol toxicity occur

A

glutathione overwhelmed, ROS produced

81
Q

epiphyses fusing in upper limb

A 
cats make rob laugh 
capitulum - 1 
med epicondyle - 5 
radial head - 5
lat epicondyle, trochlea, olecranon- 10

exam revision (15 decks)

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